A corollary of the plasticity of muscle pHi regulation evident from the training studies
reported above is that any upregulation is potentially reversible. The reversibility of training- induced adaptations (outcome) following a period of training cessation or reduced training (process) is referred to as detraining (333). The rate at which training adaptations are lost typically varies between weeks and months, depending on the mechanism investigated, with endurance adaptations seemingly more rapidly reversed (295, 347, 447).
Reductions in oxidative enzyme activity have been found 3 or 7 weeks after stopping training (11, 96, 330), whereas glycolytic enzyme activity has been shown to take between 7 weeks and 6 months to return to baseline (400, 431). Performance adaptations similarly vary in their transience, with maximal sprint power changing little 7 weeks after stopping training (295), but large reductions in maximal aerobic power and 90-s cycling performance evident over the same period (431).
Limited research has been conducted into the timecourse of the reversibility of adaptations in pHi regulation, but the evidence suggests such loss of adaptations occurs quickly.
In perhaps the first study to demonstrate the rapidity of this, 4 weeks after swimmers stopped a 5-month intensive training programme, indirect evidence of a reduction in pHi-regulatory
capacity was shown by greater blood [La−] and [H+] at the end of a performance swim (112). It is only lately that direct follow-up of the transience of adaptations in pHi regulation has been
undertaken, primarily in horses.
Apparent improvements in βmin vitro of 19% after 34 weeks of training in horses were
reported to be reversed following 12 weeks of no training (315). There was little change in βmin vitro after ~30 weeks of multiple phases of training in control and overload training groups
of horses111, but after overtraining had been identified in the overload training group at week 31, there were large increases for the subsequent data (Figure 2.16). Following 10 weeks confinement to their yards, complete loss of adaptations in βmin vitro was said to have occurred.
However, it is more likely that the large increase at 32 weeks was methodological variation, given that the control group had a similar, if not greater increase than the overload group. As such, without a clear training effect there was no clear evidence of detraining in this study.
111
The two groups of horses performed continuous training for 4 km at ~60% V̇O2max, for 7 weeks × 5 d•wk−1, followed by 9 weeks of 3 d•wk−1 moderate intensity training (3 km at ~80% V̇O2max) and 2 d•wk−1 of HIT (3 × 2 min at 100% V̇O2max). Their training then differed for the next 16 weeks, with the overload group performing HIT 3 d•wk−1 (11 wk of up to 8 × 2 min at 100% V̇O2max, followed by 5 wk of 10–15 × 1 min at 110% V̇O2max) and moderate-intensity training 3 d•wk−1 (6 km at ~80% V̇O2max), whereas the control group performed HIT 2 d•wk−1 (3–4 × 2 min at 100% V̇O2max) and moderate-intensity training 3 d•wk−1 (3.0–4.5 km at ~80% V̇O2max).
Figure 2.16 βmin vitro in horses after multiple stages of training and detraining. There were 7 weeks of
moderate-intensity training (MOD), 9 weeks of moderate and high-intensity training (MOD/HIT), 15 weeks of overload training or control, 2 weeks of reduced training, and 10 weeks of no training. Data are mean (SD). control group and overload training group. Modified from McGowan et al. (315). See text for additional details.
In the first published study investigating reversal of adaptations in any of the acid/base transporters in humans, following a 6-week period of repeated 30-s all-out sprints (1:8 work:rest), MCT1 content remained elevated one week after stopping training, but had reduced to the pre-training level after 6 weeks (79). The post-training increase in MCT4 content was reduced by 20% one week after stopping training and had fallen to the mean pre-training value after 6 weeks. An important caveat here in interpreting a potential physiological detraining response is that the individual increases in MCT1 and MCT4 content after training were highly variable, 30–530% and 15–200%, respectively (cf. Figure 2.13). Although not reported, presumably the individual detraining responses were equally varied.
Others subsequently reported no statistically significant change in MCT1 or MCT4 after two weeks of training cessation in football players following the end of their season (468). From their data it is apparent there was a progressive reduction in abundance of both proteins 3 d and 2 wk after stopping training. A detraining response probably commenced quite rapidly, but the variance meant an uncertain effect. Interestingly, the same participants demonstrated a rapid upregulation in NHE1 protein abundance upon stopping training, ~25% and ~35% increase at 3 d and 2 wk respectively, a response that was absent in a group who performed HIT over the same two-week period. It is unclear why NHE1 responded to such a reduction in training load, and whether this was simply an artefact of the high variance, but it certainly merits further investigation.
In another study with horses, a 6-week period of stall-rest following 18 weeks of high- intensity training112 saw a reversal of increases in MCT1 and MCT4 protein content, and in the important mitochondrial enzyme citrate synthase (266). MCT1 but not MCT4 content remained elevated in a parallel group that maintained a moderate level of activity for 6 weeks113. It may be that maintenance of MCT4 upregulation requires inclusion of high-intensity training to prevent rapid detraining, while improvements in MCT1 content are more readily maintained. There is some evidence suggesting that reversal of adaptations in specific physiological variables such as maximal oxygen uptake and relative substrate usage can be avoided with a reduction in both intensity and volume of training (388), but the prevailing view in maintaining training adaptations favours reducing volume, while maintaining training intensity, to prevent or mitigate physiological detraining (334, 335, 347). And there is much research to support this view (214, 215, 226, 227, 309, 427). Given that the data presented earlier suggest upregulation of the MCTs and NHE1 is typically only achieved following high-intensity training, it is likely that the removal of a high-intensity stimulus can result in a reduction of protein content. Conversely, reducing training volume but maintaining a high-intensity stimulus may be sufficient to maintain protein content. Therefore, specific data on the acid/base transport proteins and βm should help inform how best to maintain training adaptations despite a reduction in training volume.